Henry Ford Hospital Medical Journal

Volume 17 Number 4 Article 11

12-1969

"Anion-Gap Acidosis" Complicating Diabetic Ketoacidosis: A Commentary on Diagnosis and Management

J. Craig Jurgensen

Fred W. Whitehouse

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Recommended Citation Jurgensen, J. Craig and Whitehouse, Fred W. (1969) ""Anion-Gap Acidosis" Complicating Diabetic Ketoacidosis: A Commentary on Diagnosis and Management," Henry Ford Hospital Medical Journal : Vol. 17 : No. 4 , 311-314. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol17/iss4/11

This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. Henry Ford Hosp. Med. Journal Vol. 17, No. 4, 1969

NOTES AND COMMENTS I

'Anion-Gap Acidosis" Complicating Diabetic Ketoacidosis A Commentary on Diagnosis and Management

J. Craig Jurgensen, M.D. and Fred W. Whitehouse, M.D.*

A 23-year-old diabetic woman early management of any patient with a (HFH #1315375) in the seventh comparable problem. Diagnostic con­ month of her second pregnancy was siderations include: eclampsia, keto­ brought comatose to the Emergency acidosis, hypoglycemia, central ner­ Room of the Henry Ford Hospital. vous system diseases, and drug inges­ Three days previously, she had experi­ tion. A normal blood pressure and enced weakness, fatigue, and increased absence of convulsions makes eclamp­ thirst, followed by nausea and vomit­ sia unlikely. Did the initial laboratory ing. Six hours before admission she had study guide us toward the correct become unconscious. Diabetes mellitus diagnosis? was diagnosed at the time of her first The data included a hemoglobin of 16.7 pregnancy three years ago. One week gm per 100 ml and a serum urea nitrogen of 32 mg per 100 ml, while the urinalysis before the onset of this present illness, showed 4-|- glucose and acetone. The blood her private physician had reported a sugar was 315 mg per 100 ml with a serum bicarbonate of 5 mEq per liter. A determina­ normal fasting blood sugar. tion of the serum ketones was strongly positive (44-) in three successive dilutions. Physical examination showed an obese, The arterial pH was 7.22. dehydrated, unresponsive patient. Her blood pressure was 140/80 mmHg, pulse 100 per These findings support a diagnosis of minute, and temperature 100°F. Respirations were of the Kussmaul type, 40 per minute. ketoacidosis. The mere finding of Optic fundi showed no papilledema, hemor­ serum ketones does not imply a state rhages, or microaneurysms. The neck was supple. The deep tendon reflexes were hypo­ of acidosis. Acidosis does ensue with active bilaterally. The uterus was enlarged to massive ketosis and uncompensated a seven month size of gestation. base deficiency. Technically, we like to With the preceding description, a crush the reagent tablet to assure opti­ multitude of diagnoses are conceivable. mal chemical interaction. Aqueous di­ To narrow the possibilities, we need a lutions are carried out when the few modifying details. Her symptoms undiluted serum on the scale of 0-4 developed suddenly. There was no pre­ records strongly positive. A 4-\- re­ ceding fever, edema, or hypertension. action represents roughly 50 mg of Knowing these facts influences the ketones per 100 ml serum. ^ The acidemia of ketoacidosis is due Department of Medicine to excess proton-donating ketoacids.

311 Jurgensen and Whitehouse

especially beta-hydroxybutyric acid. formed early in our patient. The material Accelerated lipolysis and the conse­ aspirated was blood-flecked and copious. quent base depletion bring about the Gastric lavage lowers the chance of serious pH change we see. All the bronchial aspiration, decreases the as­ blood buffers are eventually consumed sociated gastric atony, and generally in the compensatory effort. hastens oral intake during the convales­ cent stage. Unfortunately, gastric la­ In treatment, we gave 100 units of crystal­ line insulin initially and three liters of hypo- vage is often ignored when treating this osmolar saline (230 mOsm) and 176 mEq condition. Incidently, we have shown of sodium bicarbonate. by gastrocamera that hemorrhagic gas­ Depending upon the age of the pa­ tritis is a frequent complication of tient, the duration of the diabetes, the ketoacidosis.* height of the initial blood glucose level Twenty hours after admission, we had and the degree of ketonemia, we rec­ given our patient 500 units of insulin, five liters of hypoosmolar saline, and 250 mEq ommend an initial dose of 50-100 units of bicarbonate. The blood sugar was 150 mg of crystalline insulin to patients with per 100 ml and the serum was free of ketone bodies. However, the blood CO2 remained ketoacidosis. One system for judging 8 mEq per liter and the arterial pH 7.20. the initial dose of insulin advises 50- The BUN was 30 mg per 100 ml and the rectal temperature 102°F. The blood pres­ 100 units for each strongly positive sure was 118/80 mmHg. Clinically, she was (4+) reaction in the serum ketone comatose and had dramatic Kussmaul res­ pirations. She was well-hydrated. At this test. Modesty on the first dose is cer­ time, a macerated fetus weighing five pounds tainly justifiable; the degree of effect presented in the birth canal and was de­ livered without difficulty. will be seen within two hours and can be further adjusted. Generally, when insulin resistance is Intracellular deficits in patients with overcome and the blood glucose ap­ ketoacidosis include water, salt, bicar­ proaches normal, the serum wiU be bonate, potassium and glucose.^ We free of ketones and the patient will delay the infusion of exogenous glucose show clear evidence of improvement. until an insulin effect clearly develops In our patient, metabolic acidosis per­ and the blood glucose falls below 200 sisted without ketosis. With this lack mg per 100 ml. Premature use of of response, we consider inadequate glucose only aggravates intracellular insulin, too little potassium, or cerebral dehydration and allows continuing os­ edema. motic diuresis, which accentuates po­ On further testing, we found that our patient's cerebrospinal fluid was sterile, acel­ tassium and water loss. It also spoils a lular, and of normal pressure. Blood and fine guide of insulin effect. urine cultures were negative. The fibrinogen was 130 mg per 100 ml. Urinalysis demon­ Pregnancy complicating ketoacidosis strated no sugar, casts, RBC's, or albumin. demands especially aggressive correc­ The BUN was 40 mg per 100 ml. Hourly tion of the acidotic state since acidosis output was 20 ml with blood pressure as low as 50 mmHg systolic. Aramine was is lethal to the fetus. Adequate bicar­ required for support. bonate therapy will correct the alkali Diminished glomerular filtration is deficit. The fetal mortality in any given known to occur in patients with keto­ episode of acidosis will approach acidosis.' Ordinarily this does not 50%.3 cause oliguria if hydration is main­ Gastric lavage and suctioning were per­ tained. In our patient, multiple factors,

312 "Anion-Gap Acidosis" Complicating Diabetic Ketoacidosis

including electrolyte imbalance, acido­ is maintained through the pyruvate sis, fever, shock, and a precipitous system. In class II, however, lactate f delivery contributed to the oliguria. accumulates in large amounts, con­ The serum electrolytes were: Na 145 sumes all available buffers and causes mEq/1, K 3.6 mEq/1, Cl 108 mEq/1; irreversible acidosis. arterial pH 7.20. Blood lactate was not available at this time for our use. Determination of blood lactate in our patient was not possible at this time. Be­ The difference of the sums of cations cause of her general clinical state and the and anions is normally less than 10: known association with shock, blood loss, and fever, we made a presumptive diagnosis (Na -f K) - (Cl + HCO.-, -f 12) of lactic acidosis. =^ 10. This is a raw number which Peritoneal dialysis was done, using 1.5% Impersol buffered with 44 mEq NaHCOa. tests electrochemical neutrality." The After 24 hours of dialysis, the urea nitrogen factor of 12 accounts for a group of was 20 mg per 100 ml; the arterial pH was fixed anions present in the blood. In 7.4, the serum bicarbonate 28 mEq/1. We recalculated the anion-gap as: (148-f4.0) — any case of acidosis, a "gap" will exist (1044-28-1-12) = 8. The patient was awake, in the anion side of the equation which breathing slowly, and was in metabolic bal­ ance. is filled by either ketoacids, renal acids, She went home on the fourteenth hospital or by lactic acid. This situation implies day and has been well since. an excess of H+ ions, that is, dissocia­ Recently we treated a confirmed case tive ions which characterize any acid of lactic acidosis in a similar manner by with a known dissociation constant. dialysis. This patient (HFH #1328308) Calculation of our patient's "anion- also survived despite known statistics gap" after the treatment of ketoaci­ to the contrary. In proposing this form dosis showed a figure of 32. Since of therapy, we believe the advantage lactic acidosis sometimes follows severe of dialysis is probably the massive ketoacidosis, we considered this pos­ and rapid effusion of H4- ions. This sibility. Some authors have also sug­ form of acid excretion replaces usually gested that the intrauterine dead fetus deficient renal function caused by is a potent source of lactic acid," which lowered renal perfusion. clears following delivery of the fetus. We are aware of the presence of In our patient, however, acidosis fol­ lactate in commercial Impersol. Lac­ lowed the obstetric delivery. tate is a known buffer in the salt form Lactic acidosis subsequent to poor and may act in the same way in the tissue perfusion is uniformly fatal. dialysate. The endogenous lactate acts Huckabee separates lactemia (class I) as an acid in lactic acidosis. Preferably, from lactic acidosis (class 11).^ The a bicarbonate dialyzing material would former condition is common and oc­ provide a more efficient buffering sys­ curs in many disease states. Acidosis tem, but such a material is not available does not occur because lactate disposal at this time.

REFERENCES 1. Duncan, G.G., and GUI, R.J.: Clinical value of a simple qualitative test for plasma acetone in diabetic coma. Diabetes 2:353-7, Sept-Oct 1953. 2. Stanbury, J.B.; Wyngaarden, J.B., and Fredrickson, D.S.: The Metabolic Basis of Inherited Disease, ed 2, New York: Blakiston Division - McGraw-Hill, 1966, pp 97-9.

313 Jurgensen and Whitehouse

3. Kyle, G.: Maternal diabetes and fetal survival. Ann Intern Med 59:23-32, 1963. 4. Carandang, N.; Schuman, B., and Whitehouse, F.W.: Gastrocamera in patients with diabetic ketoacidosis. Gastroint Endosc. To be published. 5. Reubi, F.: Glomerular filtration rate, renal blood flow and blood viscosity during and after diabetic coma. Circ Res 1:410-3, Sept 1953. 6. Carlson, E.E.: Lactic acidosis. Minn Med 52:655-64, Apr 1969. 7. Unpublished material. 8. Huckabee, W.E.: Abnormal resting blood lactate. II. Lactic acidosis. Amer J Med 30-840-8 Jun 1961.

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